Vaso-active mediators and doppler indices in maternal and fetal vessels in pre-eclampsia

Pre-eclampsia is associated with increased vascular reactivity and vasoconstriction. Forty six women whose pregnancy were complicated with pre-eclampsia and twenty six normotensive pregnant women all at the same duration of pregnancy were studied. Pre-eclampsia occurred in the 2nd trimester only in two patients, in the sometime it occurred in 28 patients before the 37th weeks and 16 after the 37th weeks. Only eight patients were with moderate hypertension, while 38 patients were with severe disease. Blood flow velocity waveforms in both right and left uterine arteries, fetal umbilical artery and fetal descending aorta was done for both patients and controls. Serum levels of endothelin-I [ET1], prostaglandin E2 [PGE2], nitric oxide [NO], Von Willebrand factor [vWF] and angiotensin converting enzyme activities [ACE], were determined for both patients and controls. Serum levels of ET-1, ACE and vWF were higher, while serum levels of NO and PGE2 were lower to statistically significant levels [p<0.001] in pre-eclamptic women in all instances. Also, all Doppler indices were significantly higher in patients with pre-eclampsia than in normotensive women [p<0.001]. There was strong positive correlation between Doppler indices and serum levels of ET-1, ACE and vWP and strong negative correlation with NO and PGE2 in both patients with pre-eclampsia and in normotensive women [r<0.05]. These changes confirm the presence of highlight vascular reactivity and endothelial damage in cases of pre-eclampsia. The resulting endothelial damage and dysfunction may underlay the pathologic features of this disorder

Estimation of phospholipase A2 [PLA2]. Protaglandin E2 [PGE2] cyclic amp [CAMP]. interferon - Y [IFN - Y] and soluble interleukin - 2 receptor [SiL - 2 R] levels in middle ear effusion

Levels of PLA[2]. PGE[2]. CAMP, IFN-omega and SIL-2R were estimated in middle ear effusions from 32 patients suffering from otitis media with effusion. They were 19 patients with mucoid type effusion and 13 with serous type. All parameters estimated showed significant increase in cases with mucoid effusion except level of IFN-omega which was significantly increased in the serous type and we suggested that both serous and mucoid types of otitis media with effusion may have different immunological background

Calcium and prostaglandins in blood and uterine muscle in normal and abnormal uterine actions

Uterine activity integral [UAI] together with plasma and uterine muscle calcium ions, PGF2 alpha and PGE2 were estimated in 32 primigravidae of those admitted to the Department of Obstetrics and Gynecology of El-Menia University Hospital and delivered by cesarean section. Seven women showed normal uterine action, 15 showed hypotonic uterine action, and 10 showed hypertonic uterine action. The study showed that PGE2 alpha and calcium ions levels increased in blood and uterine muscle during labor, especially in the hypertonic state and decreased in the hypotonic contractions, whereas, PGE2 showed no significant changes. These changes could incriminate PGF2 alpha and calcium ions in the pathogenesis of these abnormal uterine actions

Plasma prostaglandin E in portal hypertension: effect of suppression by indomethacin

A possible role of vasodilating prostaglandins [PGs] in the pathogenesis of circulating abnormalities of cirrhosis as well as in portal hypertension and renal function status was studied. Plasma PGE [by radioimmunoassay RIA], percutaneous trans-splenic portal manometry and 24 hours creatinine clearance [CrCl] were measured in 40 males with chronic liver disease [20 ascitics and 20 non-ascitics] before and after one day oral indomethacin 50 mg/8 hours] administration. Portal pressure [PP] was graded as moderately and severely raised. Ascitics had higher plasma PGE [P < 0.001] and lower CrCl [p < 0.01] than non-ascitics. PP was not significantly different in ascitics and non-ascitics plasma PGE was not significantly different in patients with moderate compared to those with severe portal hypertension. Indomethacin induced a reduction in PGE in both ascitics [from 6.09 +/- 0.29 to 2.83 +/- 0.43 ng/ml, P < 0.01] and non ascitics [from 4.15 +/- 0.31 to 2.87 +/- 0.29 ng/ml, P<0.001] and in patients with moderate portal hypertension [from 4.85 +/- 1.06 to 2.82 +/- 0.33 ng/ml, P < 0.001] and those with severe portal hypertension [from 5.19 +/- 1.02 to 2.85 +/- 0.38 ng/ml, P < 0.001]. PP was reduced in ascitics [from 30.2 +/- 5.23 to 26.0 +/- 4.67 cm saline, P < 0.001] and non-ascitics [from 28.05 +/- 3.96 to 25.15 +/- 3.51 cm saline, P < 0.001]. CrCl was reduced in ascitics [from 98.6 +/- 7.15 to 64.8 +/- 4.9 ml/min, P < 0.001] and non ascitics [from 105.15 +/- 7.01 to 90.5 + 6.12 ml/ mill, P < 0.001]. Plasma PGE, PP. and CrCl decrements [J] were higher [P < 0.001] in ascitics than in non-ascitics [3.29 +/- 0.42 vs 1.28 +/- 0.24 ng/ml, 4.2 +/- 1.1 vs 2.9 +/- 0.91 cm saline and 33.8 +/- 0.04 vs 14.2 +/- 3.78 ml/min, respectively]. In both ascitics and non-ascitics JPGE, JP and JCrCl were positively intercorrelated [P <0.01]. Plasma PGE contributes in the pathogenesis of portal hypertension, although it does not determine its severity. PGE synthesis inhibition by indomethacin affectively reduces PP. Adversely, it reduces glomerular filtration rate especially in ascitic patients